• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/202

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

202 Cards in this Set

  • Front
  • Back
What does pathology include?
-etiology/ cause
-pathogenesis/ mechanism
-alterations in tissue/cell
-manifestations of disease in living organism
Two major subdivisions of Human/Animal pathology
-Anatomic pathology
-clinical pathology/ laboratory
What does anatomic pathology deal with?
-changes in tissues at gross and microscopic levels
-subcellular and molecular alterations
Major sub-divisions of anatomic pathology
-surgical pathology
-cytopathology
-autopsy pathology
Two sub-divisions of autopsy pathology
-Forensic autopsy
-medical autopsy
What pathology is most common in a hospital?
surgical pathology
What do surgical pathologists do?
-examine tissue samples removed by simple biopsies or major surgeries
-use gross observations of tissue and microscopic observations to make diagnosis
-examine "frozen sections" of tissue at request of surgeons to determine nature of disease
Significance of a "frozen section"
helps the surgeon plan the method and extent of surgery
Cytopathology
deals with changes in individual cells
-cells collected as CSF, urine, and peritoneal fluid via PAP smears or FNA via fine needle
Fine needle aspiration (FNA)
biopsy technique useful when lesions are deep seated in pancreas, liver, kidney, body wall, thyroid, etc
autopsy pathology
-deals with examination of whole body after death
-external examination first , then internal
medical autopsy
-concerns with patients who have died of medical or natural causes without any evidence of suicide or a crime.
-helps determine of quality and accuracy of care
-major tool for effect of diseases on body
Forensic autopsy
-deals with cause and manner of death in sudden or violent cases
What guides the anatomic pathologist to a diagnosis
the pattern of changes in the tissue and cells
Clinical pathology
-lab and microbiological testing important for day to day patient care
-examination of blood, CSF, body fluids, analysis of stones,etc
What does a forensic pathologist do?
-inspect crime/accident scene
-documents external evidence
-dissects organs and tissues to identify cause of death
-orders lab tests to check for drugs, toxins, chemicals
-report to identify cause, manner, and mechanism of death
Cause of death
disease or injury that initiates the train of events leading to death
Mechanism of death
disturbances in physiologic and biochemical state that follows the cause of death
-ex exsanguination(draining of blood) is cause of death, but can be caused from bullet wound, MVA, spontaneous rupture ( mechanisms of death)
Manner of death
tells how the cause of death came about
S-suicide
H-homocide
A-accidental
U-undetermined
N-natural
Best ways to determine death ranked in order of best to least
1. eyewitness
2. algor mortis ( drop in body temperature)
postmortem interval
time of death and the interval since death
rigor mortis
right after death , the 12- hour progressive depletion in ATP resulting in muscles and joints stiffening up
-lasts another 12 hours once maximized
-by 36th hour of postmorten, muscle stiffness diminishes
livor mortis
the settling of blood
K+ levels after death
levels in vitreous humor has steady linear rise due to loss of Na+/K+ pumps in dying cells
Testing of CO in autopsy
- if sufficient CO inhaled, will have bright red blood and "cherry red" tisue/skin color
homeostasis
steady state that can withstand normal physiological demands.
What are 2 forms of visible signs of stress on a cell?
1. intracellular accumulations
2. cellular aging
adaptation
occurs in response to increased demand, decreased demand or chronic irritation
hyperplasia
a cells response to increased demand through increasing the NUMBERs of cells
hypertrophy
a cells response to increased demand through increasing the size of cells
atrophy
cells response to decreased demand through diminution in size
What are some ways cells are stimulated to undergo atropy
-decreased workload
-loss of innervation
-diminished blood supply
-atherosclerotic plaque
-inadequate nutrition
-loss of endocrine stimulation
-aging
-pressure( tumor)
metaplasia
a cells response to chronic irritation by replacing one adult cell type with another
when is adaptation pathologic
when it is a response to a harmful or potentially harmful stimulus
Is the hyperplastic response of the endometrium to hormonal stimulation during the menstrual cycle pathologic or physiologic
Physiologic! because the stimulus is not harmful
Is the hyperplasia of endometrium in a postmenopausal woman resulting in post menopausal bleeding pathologic or physiologic
pathologic!
cell injury
when an injurious stimulus is severe or the cel has exceeded its ability to adapt
reversible cell injury
the cell has the potential to return to normal structure and function if the injurious stimulus is withdrawn
irreversible cell injury
leads to cell death by necrosis or apoptosis
Stimuli that can cause cell injury
-oxygen deprivation, physical agents, chemical agents, infectious agents, genetic derangements, nutritional imbalances
hypoxia
insufficient oxygen delivery to the tissues
ischemia
insufficient blood supply to the tissues
cellular processes disrupted during cell injury
-generation of ATP
-integrity of mitochondria
-transmemrane calcium homeostasis
-protection against oxidative stress
calcium homeostasis
-Ca+2 is sequestered in the mitochondria and ER
-higher outside cell than inside cell
-injury causes leakage and activates enzymes to break apart functional elements of cell
oxidative stress
formation of oxygen derived free radicals such as OH, H2O2, O2, NO
-causes disruption of membrane lipids
-denaturation of proteins
-breaks in DNA
antioxidants
molecules that scavenge oxygen derived free radicals
free radical
a molecule with an unpaired electron in its outer orbit
reversible injury
ATP production production is decreased, cell membrane may be damaged, damage to nucleic acids, but cell can recover
irreversible injury
cell has sustained persistent severe damage so that energy can no longer be produced or the cell membrane, cytoskeleton, protein machinery, or nucleic acids are damaged beyond repair
what are 2 changes that characterize irreversible injury
1. mitochondrial fxn
2. membrane integrity cannot be restored
hydropic change
vascular degeneration. the ER is distended or swollen
cell death
when cells undergo irreversible cell injury
1. necrosis
2. apoptosis
necrosis
cell death secondary to an irreversible injury
-tissue destruction by endogenous enzymes
-inflammatory response
apoptosis
"programmed cell death"
-cell is induced to dismantle its metabolic, synthetic and genetic machinery secondary to a specific internal or external message
-cleared from tissue by phagocytes
-no inflammatory response
caspases
enzymes that digest the cytoskeleton and activate endonucleases enzymes that digest the intranuclear contents including nucleic acids and their proteins
dystrophic calcification
-sign of cell injury
--necrosis
-phosphate binds to Calcium and crystals form
mutation
A variation in a DNA sequence which changes the sequence or number of amino acids in the protein product.
-Often results in a change in the function of the
protein.
- Some functional changes result in, or predispose to, disease
polymorphism
a variation in the DNA sequence that does not appear to have a major effect on the structure or function of protein product
-minor effects may alter protein function and rate of transcription, effeciency of splicing, etc
epigenetic factors
alterations in genes which do not affect the DNA sequence
ex. methylation of cytosine nucleotides
simple traits
determined by a single gene
complex traits
determined by multiple genes
-often in combination with environmental factors
qualitative traits
either present or absent
penetrance
proportionate of people with specific genotype who exhibit the associated phenotype. ex incomplete penetrance= skipping generation
qualitative traits
either present or absent
-confounded with incomplete penetrance or variable expressivity
quantitative traits
vary in a measurable way ex height, intelligence, pigment, blood pressure
-often follow a threshold model
single gene disorders
-phenulketonuria
-cystic fibrosis
-hemochromatosis
-sickle cell anemia
-thalassemia
-huntington disease
-marfan syndrome
-muscular dystrophies
contiguous gene syndromes
disorders caused by absence or dysfunction of a series of genes which are clustered together on the same chromosome
ex, Williams syndrome-chromosome 7
Williams Syndrome
- 1/10,000
-short stature
-developmental delay and intellectual disability
-typical anxious, over friendly personality
aneuploidy
wrong copy of chromosomes
Turner Syndrome (Monosomy X)
-most cases in females
-abnormal ovaries, infertile
-short stature
-hearing, heart, kidney problems
multifactorial
the interaction of multiple predisposing genes and environmental factors accounts for most common medical conditions and cancers
How do genes affect the course of disease
-likelihood of getting disease
-severity
-rate of progression of degenerative diseases
-risks of specific complications
-response to therapies
-complications of therapies
imprinting
differential function of a gene depending on its parental origin
uniparental disomy
both members of a chromosome pair inherited from the same parent
anticipation
increasing severity of effects of a mutation in successive generations
predictive testing
testing used to identify a disease causing or predisposing mutation in an individual who shows no signs of the disease
nature
predetermined, unalterable, presumably genetic
nurture
extrinsic, variable, and changeable, involves biological, social, and educational experiences
epidemiology
the study of the distribution and determinants of health and diseases, morbidity, injuries, disability, and mortality in populations
-examines structural and functional factors that influence health and disease
underlying causes of death
disease or condition that initiated the train of morbid events leading directly to death
contributing factors
factors that led to the underlying cause of death
Epidemiology is considered looking ______ to determine causes of diseases
upstream
ex. What are causes of heart disease, types of treatments effective for breast cancer, why do people smoke and others don't
what factors are compared in epidemiology
risk of disease in those exposed to some factor compared to risk among those not exposed.
ex. risk of lung cancer in those who smoke versus those who don't
cohort studies
measure factors at baseline, and then follow people over a long period of time to compare the risk of disease among those who have a factor, compared to those who do not
risk
probability of developing a condition over tie (incidence)
relative risk
ratio of risk in one group compared to another
risk exposed/ risk unexposed
attributable risk
the proportion of disease caused by a certain risk factor
What is one way that epidemiology considers how health can be determined
the "continuum" of disease that considers disease development over time
health
absence of disease, a state of complete physical, mental, and social well-being
risk factors
qualities, behaviors, agents, or hazards that could reduce health or cause disease or injury ex...riding without a seatbelt in a car
diseases
pathological conditions resulting from infection, genetics, environmental stress, etc and have an identifiable group of signs and symptoms
proximate (immediate) causes of death
finally lead to death as in heart disease or cancer. these are disease focused and based on an understanding of pathology
non-proximate(actual) causes of death
factors that increase liklihood of experiencing one of the proximate causes of death. risk factors for diseases.
-called "upstream" causes of death
healthcare
working downstream to prevent, detect, and cure disease
basic science
understanding mechanisms of the disease process
primary prevention
reduces the risk of developing risk factors
ex. offering healthy foods in schools, increasing price of cigarettes
secondary prevention
reduces risk of developing disease among people who have risk factors for that disease
ex. aspirin in those at risk for heart attacks
tertiary prevention
reduces risk of dying of an established disease
ex. treating complications of diabetes
public health
working upstream to assure conditions so that people can be healthy
which model is the "onion" model for public health
Social Ecological model
What does the hemostatic system do
prevents bleeding, maintains fluidity of blood, and allows wound healing
fibrin
polymerizes to form a glue-like coating around a platelet plug
plasmin
dissolves fibrin clot (aka fibrinolysis)
The lower the platelet count , the _(more/less)____ bleeding is likely
more
what is the usual result if a clot is big enough to block an artery and stop blood flow into a tissue
infarction
how does the hemostatic system prevent bleeding
requires rapid formation of mechanically sound clot at sites of vascular injury.
how does the hemostatic system maintain fluidity of blood
-clot formation limited to areas of injury
-forming clots on normal uninjured tissues leads to thrombosis, interruption of blood flow, and tissue death(infarction)
how does the hemostatic system allow wound healing
-framework for healing process
-clot replaced by connective tissue
Components of hemostatic system
blood vessels, platelets, coagulation factors( blood proteins), thrombolytic system
inner endothelial surface of Blood vessels
normally prevents clotting
subendothelial connective tissue of blood vessels
"matrix" that promotes clotting when exposed to blood by injury to overlying endothelium
smooth muscle cells in blood vessels
cause constriction after injury
megakaryocyte
small cell fragments derived from bone marrow
platelets
- normally 150 to 450,000 microliters of blood (1/10 as many red cells)
-circulate passively in blood until clotting process initiated
coagulation factors(blood proteins)
most are manufactured in the liver, except for vWF/factor 8
-inactive until clotting begins
-form fibrin clot
thrombolytic system( aka fibrinolytic)
dissolves clots
-released in response to clot formation
-lyses fibrin
Normal clotting process
1. injury exposes tissue
2. platelets adhere and provide surface for fibrin formation
3. coagulation factors form fibrin on platelet plug
4. vessels constrict to limit blood flow
5. clot dissolved by fibrinolytic system and replaced by connective tissue
what do platelets do
adhere to damaged blood vessels (subendothelial matrix)
-requires vWF(von Willebrand Factor) which is made by endothelial cells and secreted into blood and subendothelium
1st step of hemostasis: platelet adhesion
vWF binds platelets to exposed collagen in subendothelial matrix
Activation in platelets is triggered by
substances in subendothelial matrix such as collagen
Aspirin
partially and irreverisibly blocks activation process of platelets
What triggers aggregation of platelets
substances released from adherent platelets
- platelets stick together via blood proteins such as fibrinogen
What causes vessel constriction
substances released by platelets
Purpose of platelets membrane surface
provide site for assembly of coagulation cascade components and formation of fibrin.
ex platelets are the bricks and fibrin is the cement that holds them together
How do platelets help a clot to retract
individual platelets contract, causing whole clot to shrink and draw edges of wound together
Tissue factor
triggers coagulation cascade by binding factor 7a
Activation of coagulation cascade
-series of linked enzymatic reactions
-many of coagulation factors need vitamin K for synthesis
-only fxns on membrane surface( platelet plug surface)
Thrombin
converts blood protein fibrinogen to fibrin
fibrin
polymerizes to form a glue-like coating around the platelet plug
-main clot component
Fibrinolysis
1. Clot formation stimulates plasminogen activators
2. Plasminogen converted to active form plasmin
3. Plasmin dissolves clot
antithromnin
inhibits thrombin and other coagulation enzymes
-activity is increased by heparin
Protein C
degrades coagulation factors 5 and 7
Protein S
Cofactor for protein C
Thrombocytopenia
low platelet count due to blood loss, less production, and increased destruction of platelets
Immune thrombocytopenic purpura (ITP)
autoimune; immune system makes antibodies that stick to platelets which are then destroyed in the spleen
-may resolve in children
-need spleen removed most likely in adults
-drugs may stick to antibodies as in heparin induced
Quaitative platelet disorders
platelet count normal but platelet function abnormal
-rarely inherited
-Aspirin and other drugs that inhibit platelet fxn
-Uremia-kidney failure, toxins block fxn
Hemophilia
-A &B types
-deficiency of clotting factor 7 or 9
-causes defective fibrin formation
-only on X chromosome( leads to X linked recessive inheritance in males)
-women usually just carriers
Von Willebrand disease
-most common inherited bleeding disorder
-platelets less able to stick to damaged blood vessels to initiate clotting
-autosomal dominant inheritance
How does liver disease affect coagulation
most coagulation factors are made in the liver.
-When liver is not fxn properly, get decrease in these factors
-cause bleeding
What causes vitamin K deficiency
-produced in gut, so antibiotic use, poor diet, newborns ( b/c haven't eaten yet)
-bile acids needed to absorb vit k so any deficiency in that
Importance of Vit K
synthesis of several clotting factors require vit K
Warfarin
-blocks effect of vitamin K
-anticoagulant(blood thinner)
Heparin
-anticoagulant( blood thinner)
-to treat heparin overdose, give protamine sulfate
-treating with frozen plasma makes it worse because plasma has antithrombin and heparin enhances it effect
Intravascular fibrin formation
may cause thrombosis in small blood vessels and tissue injury
Predisposing factors for thrombosis(clot formation)
-Blood vessel or endothelial cell injury
-stasis of blood(slowing or stopping of blood flow)
-hypercoagulability( increased tendency of blood to clot)
Arterial thrombosis
-vessel injury or artherosclerosis are causes
-if clot blocks blood flow into tissue, causes tissue death and infarction
Venous thrombosis
-mostly caused by hypercoagulaton states
-blockage prevents or slows outflow of blood
-leads to tissue swelling, pain, calor as in deep vein thrombosis
-infarction less common
Embolism
blood clot breaks loose from site of origin and travels with blood flow until reaches vessel too small to pass through
-causes stroke if travels to brain
venuous emboli
usually originate in the large veins of the legs and travel through the heart into the lungs
innate immunity
non specific or generic defense mechanisms that protect the body from a wide variety of potentially injurious agents
acquired immunity
highly regulated response of the body to infectious agents it has been exposed to
2 systems innate immunity is comprised of
1. mechanical barriers-physical structures that keep the outside out and the inside in. ex... skin, mucous membranes, acidity of stomach

2. inflammation-tightly regulated response to injury by blood vessels and blood cells
what happens when the tissue senses injury
blood flow increased to area, large number of white blood cells that contain toxic molecules get out at sight of injury.
-through non specific process, offending agent cleared from the tissue and the tissue is prepared for repair
cardinal signs of inflammation
redness, swelling, heat and pain
acute inflammation general definition
inflammatory process tat is of immediate onset and relatively short duration
chronic inflammation
a process that persists for weeks, months, years
vascular phase of acute inflammation
post capillary venules dilate and cause blood flow through capillary bed to become sluggish or stagnant
stasis
pooling of blood in the capillary bed
vasoactive mediators
cause postcappilary venules to dilate
ex. histamine

-cause endothelial cells to pull apart
-leads to plasma oozing out and causes edema(swelling)
histamine
vasoactive mediator that is stored in mast cels
- released by mast cell during injury
-causes vessels in vicinity to dilate
cellular phase of acute inflammation
-white blood cells leave circulatory system, move to site of injury, become activated
-neutrophils pushed to periphery of blood when blood slows down in capillary bed , come in contact with endothelial cells
-neutrophils attach to receptors on endothelial cells and become firmly attaced
-neutrophils wiggle through gaps and get out into blood stream of tissue
-
chemotaxis
chemicals released at site of injury form a chemical gradient for neutrophils to move along
when do neutrophils become activated
once at the site of injury
-inactive when circulating in the blood stream
lysosomes
vessicles that hold toxic enzymes of neutrophils
-stimulated for release when come into contact with injured tissue
Process of neutropils
-special receptors to recogonize foreign substances
-engulf foreign molecules through phagocytosis
-
opsonins
enhance recogonition of foreign material by neutrophils
-ex antibodies
abscess
localized area of completely dissolved tissue secondary to acute inflammatory damage
-contains pus
pus
debris of dead neutrophils and liquefied tissue
plasma derived mediators of inflammation
proteins of the compliment and clotting cascades
-formed by liver, circulate in blood at high concentrations in inactive form
-form cascades of activation
-pro inflammatory effects
aggregate to form channel that plugs into bacterial walls and disrupts integrity so bacteria die
-
cell derived mediators of inflammation
-arachidonic acid metabolites: formed from lipids in cell membrane once inflammatory cell activated
steriod and NSAIDs
inhibit production of arachidonic acid metabolites and intefere with inflammatory process
macrophages
-increase at site as neutrophils die off
-made from bone marrow
-capable of phagocytosing and digesting foreign molecules
-called monocytes while circulating in blood
-prepare tissue for repair
-link acute inflammatory to acquired immune response
myofibroblasts
migrate into area and lay down collagen for repair
granulation tissue
tissue at site of injury that consists of macrophages, myofibroblasts, tangle of new blood vessels, and disorganized collagen.
cytokines
released by macrophages
-cell derived mediators of inflammation
-most important : IL-1, Il-6, and TNF-alpha
-responsible for acute phase reaction ( fatigue, anorexia, increased sleep , etc in colds)
cachexia
severe wasting due to production of cytoknes as in what occurs in TB
antigen
products of degradation from macrophages
unlike neutrophils, macrophages __________
present antigens to lymphocytes so that it can be recognized as a foreign molecule
helper T cell
carries a receptor on its cell surface that is capable of recogonizing antigen displayed on surface of macrophage
-activated if receptor fits antigen on macrophage
-secretes cytokines
-communicates with cytokines to detect that particular antigen and destroy
B-Cells
communicate with helper t-cells if substance is in ECM to produce antibodies
-b cells are lymphocytes expressing antibodies on cell surface
How do B cells operate
when an antigen matches an antibody on their cell surface they engulf it and re-express it on their cell surface
-activated by helper t cells if antigen expressed matches receptor on t cells
-differentiates into plasma cells
plasma cells
-each plasma cell produces 1 type of antibody
-antibodies recognize antigen from which it originally came and target it for degradation
-increases ability of neutrophils to recognize foreigns
what activates cascade of complimenting proteins
antibody-antigen complex
cytoxic t cells
recognize foreign antigens on the surfaces of native tissues that have become infected
-induce apoptosis
-required help from helper t cells
chronic inflammation is mediated by______
lymphocytes
granuloma
collection of macrophages, surrounded by chronic inflammatory cells, that keeps a foreign substance sequestered in one area
-contains offending agent that macrophages are not equipped to eliminate or kill
incomplete penetrance
have the gene, but dont express it
variable expressivity
have the gene but shows different in different people. Example, severity may vary from person to person
suppurative/ purulent inflammation
production of large amounts of pus composed of neutrophils, necrotic cells, and edema fluids
-response to pus forming bacteria
Steps in the process of repair
1. inflammation
2. angiogenesis- growth of new blood vessels
3.migration and proliferation of fibroblasts
4.scar formation
5. connective tissue remodeling
non specific chronic inflammation
-involves macrophages, lymphocytes, plasma cells
-tissue destruction
-fibrosis
what is the primary cell involved in chronic inflammation
lymphocyte
granulomatus inflammation
-a collection of activated macrophages
- surrounded by collar of lymphocytes
-limited differential diagnosis: infectious ( TB,leprosy, etc) cat scratch disease, foreign objects
what does the granuloma contain
the injurious agent
-walled off so it cannot be spread to other sites
humoral immunity
-B cells, antibodies
-protects against extracellular microbes
cell mediated immunity
-T cells
-protects against intracellular microbes (viruses)
What do macrophages do after they digest an antigen
-chew it up and show pieces of it on the outter part of its' cell
-travels to lymph nodes and presents it to t cells
-t cells differentiate into either helper or cytotoxic
-move to site of injury; have different effects depending on if it is helper cell or cytotoxic cell
cytotoxic effect
lyses or kills the infected cell it encounters
xylene
tissues sample placed in this
-solvent capable of dissolving parafin
the dark blue hemotoxylin is a ______ dye
basic
-has affinity to DNA and RNA so they stain dark blue to purple with this dye
red eosin
acidic dye
-has affinity for basic molecules; majority of proteins in cytoplasm
-makes red blood cells stain bright red
Major steps in tissue preparation
1.tissue fixation in 10% formalin
2.tissue processing using alcohol for dehydration and xylene for parafin infiltration
3.paraffin embeddig
4.sectioning of paraffin embedded tissue and placement on glass slide
5. deparaffinizing and rehydrating tissue section on glass slide
6.staining using Hemotoxalyn and Eosin
7. dehydration of tissue
8.placement of permount glue and coverslip ( thin piece of glass)